Since there is evidence that both the MAPK and NF-κB systems can be activated by oxidative stress in gentamicin-treated animals, the expression of p-p38 MAPK and NF-κB in the kidney during the evolution of tubulointerstitial nephritis and its relationship with histological features and renal function was investigated in gentamicin-treated rats in the presence or absence of an NF-κB inhibitor. The gene discussed is NFKB1; the disease is interstitial nephritis.